Quality control (QC) of biospecimens from oral and maxillofacial tumors patients constitutes a critical foundation for the prevention, diagnosis, treatment, and precision medicine research of these diseases. Biospecimen quality directly governs the discovery and validation of disease biomarkers, the elucidation of pathogenesis, and the efficacy of clinical translation. QC spans the entire biospecimen lifecycle—encompassing collection, processing, storage, transportation, and utilization. Its primary objectives are to ensure sample integrity, reliability, traceability, and consistency, thereby guaranteeing the robustness of research data; the accuracy of molecular subtyping, biomarker identification, and treatment response prediction; and the precision of clinical decision-making. However, current QC frameworks for these biospecimens remain underdeveloped. Drawing on domestic and international technical standards, regulatory guidelines, and recent research advances, this paper elaborates on the importance of implementing a QC management system throughout the biospecimen lifecycle. It focuses on QC methodologies tailored to diverse biospecimen types, examining how standardized sampling procedures, regulated preprocessing workflows, and optimized long-term storage conditions influence sample quality. We aim to provide concrete guidance and a transferable paradigm for establishing standardized QC protocols and an informatics-enabled traceability system specific to oral and maxillofacial tumors. Such efforts are intended to enhance the research value and clinical utility of these biospecimens, furnishing reliable sample resources and technical support for the development of precision diagnostics and therapeutics. Furthermore, we advocate for a dual-track “QC plus Ethics” management framework within biobanks. This approach would reinforce ethical and legal safeguards, establishing a robust barrier to support safe scientific innovation and clinical translation.

ObjectiveTo evaluate the predictive value of six surrogate indices of insulin resistance （IR） for cardiovascular disease （CVD） risk in adults with cardiovascular-kidney-metabolic syndrome （CKM） stages 0-3. MethodsRelated data of 6 813 participants from the China health and retirement longitudinal study （CHARLS） were analyzed. Cox proportional hazards models and restricted cubic spline （RCS） analyses were performed to evaluate the associations between six insulin resistance surrogate indices （TyG， TyG-BMI， TyG-WC， TyG-WHtR， TyG-CVAI， CVAI） and CVD incidence. Predictive performance of 6 indices was comprehensively compared from 3 dimensionalities， using receiver operating characteristic （ROC） curves for discriminative ability， net reclassification improvement （NRI） for incremental predictive value， and decision curve analysis （DCA） for clinical utility. ResultsAll six IR surrogate indices significantly predicted CVD in the CKM population. RCS analysis revealed linear associations between each index and CVD incidence. ROC analysis showed that CVAI had the highest AUC （0.628，95%CI： 0.611-0.646）， significantly outperforming the single TyG index （P=0.001 6）. NRI analysis indicated significant reclassification improvement for the event group with CVAI （event NRI=0.042 8）. DCA demonstrated that CVAI achieved the highest net benefit across most thresholds. Subgroup analysis confirmed stronger associations between CVAI and CVD risk in CKM stages 2-3. ConclusionsThese six IR surrogate indices serve as valuable tools for predicting CVD incidence in individuals with CKM stages 0-3. Among them， CVAI exhibits optimal predictive value for future CVD risk in adults with CKM stages 1-3.

Objective To explore the pathogenesis and prognostic factors of liposarcoma in the head and neck region, and simultaneously analyze the efficacy of different treatment regimens. Methods A retrospective analysis was performed on all patients with primary untreated head and neck liposarcoma who were diagnosed and underwent surgical treatment at our hospital from January 2008 to January 2024. All patients were monitored during follow-up, and their prognoses were analyzed using SPSS software. Results A total of 30 patients were included in the study. Liposarcoma accounted for up to 60% of the cases in the orbit, while the remaining liposarcomas were primarily located in various interspaces of the neck. Dedifferentiated liposarcoma was the most common type, comprising 33%, while myxoid pleomorphic liposarcoma was the rarest at 4%. The tumor pathological type (P<0.001) and Ki67 (P=0.014) significantly affected the tumor control rate. However, an analysis of disease-specific survival rates revealed no significant differences across various factors (all P>0.05). Conclusion The prognosis of head and neck liposarcoma is better compared to that of liposarcomas in other parts of the body. However, myxoid pleomorphic liposarcoma, pleomorphic fat sarcoma, and high Ki67 levels are indicators of poor prognosis. Additionally, postoperative adjuvant radiotherapy does not significantly enhance disease-specific survival rates.

OBJECTIVE To investigate the prognostic factors of chondrosarcoma of the larynx,deeply analyze its clinical data,and provide a theoretical basis for better treatment of chondrosarcoma of the larynx.METHODS A retrospective analysis was conducted on the complete clinical data of patients with primary chondrosarcoma of the larynx admitted to the Department of Otolaryngology Head and Neck Surgery,Beijing Tongren Hospital,Capital Medical University from January 2010 to December 2024.RESULTS A total of 15 patients were included,including 11 males and 4 females,with a gender ratio of 11∶4.The average age of onset was 57.3 years,and the average clinical symptom duration was 12.2 months.The tumors were mainly located in the cricoid cartilage in 11 patients,in the arytenoid cartilage in 2 patients,and in the thyroid cartilage in 2 patients.Tumor grading showed that 7 patients were grade I and 8 were grade II.Four patients underwent transoral laser minimally invasive surgery,2 patients underwent partial laryngectomy+tracheotomy,and 9 patients underwent total laryngectomy/cervical lymph node dissection+tracheostomy.The 5-year overall survival rate was 85.7%,the 5-year disease-specific survival rate was 100%,and the 5-year local-regional control rate was 90.9%.Gender,tumor location,tumor grade,Ki-67,tumor size,and whether larynx preservation surgery was performed did not affect the local-regional control rate or disease-specific survival rate.CONCLUSION Laryngeal chondrosarcoma generally has a longer disease history and is difficult to detect.The pathological type is mostly well-differentiated.Regional or distant metastasis is rare,and the long-term survival rate is good.Surgical resection is the preferred treatment option.On the basis of not reducing the tumor control rate,surgery that prioritizes preserving laryngeal function should be given priority,while comprehensive treatment is generally not recommended.

Objective:To explore the role and related mechanism of myeloid related differentiation markers (MYADM) in lung adenocarcinoma metastasis induced by high cholesterol diet.Methods:(1) Cell experiments: Using lung adenocarcinoma A549 and H1975 cells, the cells were treated with 0.8 mg/ml cholesterol and then transfected with a lentivirus to knock down MYADM. The overexpression of MYADM was achieved by transfecting the cells with an overexpression plasmid. Western blotting was used to detect the expression levels of MYADM, E-cadherin, β-catenin, MMP-2, MMP-9, and vimentin in the cells. The proliferation ability of the cells was assessed using the plate clonal formation assay, while the migration and invasion ability were evaluated using the Transwell assay. Western blot was used to determine the effects of MYADM knockdown or overexpression on these proteins. Western blot and immunofluorescence assays were conducted to investigate the impact of Akt phosphorylation on the expression of MYADM and Rac1 in cholesterol-treated lung adenocarcinoma cells, as well as the phosphorylation of c-Myc. Western blot was also used to assess the effect of c-Myc knockdown on the expression of MYADM and MCT1 in lung adenocarcinoma cells. Chromatin immunoprecipitation (ChIP) assays were performed to investigate the impact of cholesterol on the binding between c-Myc and the promoters of MYADM and MCT1 in lung adenocarcinoma cells. (2) Animal experiment: A549 cells or A549 cells with MYADM knockdown were intravenously inoculated into BALB/c nude mice, which were then divided into a normal diet group and a high cholesterol diet group. Using a live imaging system, the growth and metastasis of tumors in the mice were monitored. After 42 days, lung tissues were collected for immunohistochemical staining to detect changes in relevant proteins.Results:After cholesterol treatment, the expression level of MYADM in A549 cells increased from 1.00±0.18 to 3.28±0.28 ( P<0.001), and in H1975 cells, it increased from 1.00±0.06 to 2.03±0.10 ( P<0.001). Compared with the control group, the expression of E-cadherin in lung adenocarcinoma cells after MYADM knockdown increased ( P<0.01), while the expressions of β-catenin, MMP-2, MMP-9, and vimentin decreased (all P<0.01). After MYADM knockdown, the number of clonal plates decreased in A549 cells (203±23 vs 60±18, t=8.48, P=0.001) and H1975 cells (298±64 vs 137±51, t=3.41, P=0.271). The number of invasive cells also decreased in A549 cells (212±18 vs 99±34, t=5.09, P=0.007) and H1975 cells (268±34 vs 134±14, t=6.31, P=0.003). Additionally, the number of migratory cells decreased in A549 cells (353±37 vs 124±29, t=8.44, P=0.001) and H1975 cells (279±41 vs 79±19, t=7.67, P=0.002). In the lung adenocarcinoma cells overexpressing MYADM, the expression of E-cadherin decreased ( P<0.01), while the levels of β-catenin, MMP-2, MMP-9, and vimentin increased (all P<0.01). The number of plate clonal colonies formed by lung adenocarcinoma cells overexpressing MYADM increased significantly in A549 cells, (94±26 vs 298±34, t=8.26, P=0.001) and H1975 cells (83±13 vs 331±24, t=15.74, P<0.001). The number of invasive A549 cells also increased (118±17 vs 193±24, t=4.41, P=0.012) and (156±19 vs 321±12, t=12.72, P<0.001). Additionally, the number of migrating cells increased in A549 cells (171±22 vs 284±15, t=7.35, P=0.002) and in H1975 cells (178±7 vs 263±12, t=10.6, P<0.001). Experiments related to the molecular mechanism showed that overexpression of MYADM promotes the expression of MCT1 in lung adenocarcinoma cells (all P<0.01). Cholesterol not only enhances the expression of MYADM in lung adenocarcinoma cells, but also boosts the expression of Rac1 and MCT1, as well as the phosphorylation of Akt and c-Myc (all P<0.05). Immunoprecipitation experiments revealed that in A549 cells treated with cholesterol, MYADM-Rac1 interaction levels increased from (100.0±15.9)% to (191.0±26.7)% ( P=0.007), while in H1975 cells, the levels increased from (100.0±18.2)% to (170.0±27.5)% ( P=0.021). ChIP confirmed that cholesterol treatment enhances the binding of c-Myc to the promoters of MYADM and MCT1. In vivo experiments demonstrated that a high-cholesterol diet promotes the metastasis of lung adenocarcinoma cells in mice, inducing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissue. Conversely, knocking down MYADM inhibits the metastasis of lung adenocarcinoma cells in mice, suppressing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissues. Conclusion:Cholesterol may induce lung adenocarcinoma cells proliferation and metastasis by regulating the MYADM/Rac1/Akt/c-Myc/MCT1 axis.

Objective:To explore the role and related mechanism of myeloid related differentiation markers (MYADM) in lung adenocarcinoma metastasis induced by high cholesterol diet.Methods:(1) Cell experiments: Using lung adenocarcinoma A549 and H1975 cells, the cells were treated with 0.8 mg/ml cholesterol and then transfected with a lentivirus to knock down MYADM. The overexpression of MYADM was achieved by transfecting the cells with an overexpression plasmid. Western blotting was used to detect the expression levels of MYADM, E-cadherin, β-catenin, MMP-2, MMP-9, and vimentin in the cells. The proliferation ability of the cells was assessed using the plate clonal formation assay, while the migration and invasion ability were evaluated using the Transwell assay. Western blot was used to determine the effects of MYADM knockdown or overexpression on these proteins. Western blot and immunofluorescence assays were conducted to investigate the impact of Akt phosphorylation on the expression of MYADM and Rac1 in cholesterol-treated lung adenocarcinoma cells, as well as the phosphorylation of c-Myc. Western blot was also used to assess the effect of c-Myc knockdown on the expression of MYADM and MCT1 in lung adenocarcinoma cells. Chromatin immunoprecipitation (ChIP) assays were performed to investigate the impact of cholesterol on the binding between c-Myc and the promoters of MYADM and MCT1 in lung adenocarcinoma cells. (2) Animal experiment: A549 cells or A549 cells with MYADM knockdown were intravenously inoculated into BALB/c nude mice, which were then divided into a normal diet group and a high cholesterol diet group. Using a live imaging system, the growth and metastasis of tumors in the mice were monitored. After 42 days, lung tissues were collected for immunohistochemical staining to detect changes in relevant proteins.Results:After cholesterol treatment, the expression level of MYADM in A549 cells increased from 1.00±0.18 to 3.28±0.28 ( P<0.001), and in H1975 cells, it increased from 1.00±0.06 to 2.03±0.10 ( P<0.001). Compared with the control group, the expression of E-cadherin in lung adenocarcinoma cells after MYADM knockdown increased ( P<0.01), while the expressions of β-catenin, MMP-2, MMP-9, and vimentin decreased (all P<0.01). After MYADM knockdown, the number of clonal plates decreased in A549 cells (203±23 vs 60±18, t=8.48, P=0.001) and H1975 cells (298±64 vs 137±51, t=3.41, P=0.271). The number of invasive cells also decreased in A549 cells (212±18 vs 99±34, t=5.09, P=0.007) and H1975 cells (268±34 vs 134±14, t=6.31, P=0.003). Additionally, the number of migratory cells decreased in A549 cells (353±37 vs 124±29, t=8.44, P=0.001) and H1975 cells (279±41 vs 79±19, t=7.67, P=0.002). In the lung adenocarcinoma cells overexpressing MYADM, the expression of E-cadherin decreased ( P<0.01), while the levels of β-catenin, MMP-2, MMP-9, and vimentin increased (all P<0.01). The number of plate clonal colonies formed by lung adenocarcinoma cells overexpressing MYADM increased significantly in A549 cells, (94±26 vs 298±34, t=8.26, P=0.001) and H1975 cells (83±13 vs 331±24, t=15.74, P<0.001). The number of invasive A549 cells also increased (118±17 vs 193±24, t=4.41, P=0.012) and (156±19 vs 321±12, t=12.72, P<0.001). Additionally, the number of migrating cells increased in A549 cells (171±22 vs 284±15, t=7.35, P=0.002) and in H1975 cells (178±7 vs 263±12, t=10.6, P<0.001). Experiments related to the molecular mechanism showed that overexpression of MYADM promotes the expression of MCT1 in lung adenocarcinoma cells (all P<0.01). Cholesterol not only enhances the expression of MYADM in lung adenocarcinoma cells, but also boosts the expression of Rac1 and MCT1, as well as the phosphorylation of Akt and c-Myc (all P<0.05). Immunoprecipitation experiments revealed that in A549 cells treated with cholesterol, MYADM-Rac1 interaction levels increased from (100.0±15.9)% to (191.0±26.7)% ( P=0.007), while in H1975 cells, the levels increased from (100.0±18.2)% to (170.0±27.5)% ( P=0.021). ChIP confirmed that cholesterol treatment enhances the binding of c-Myc to the promoters of MYADM and MCT1. In vivo experiments demonstrated that a high-cholesterol diet promotes the metastasis of lung adenocarcinoma cells in mice, inducing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissue. Conversely, knocking down MYADM inhibits the metastasis of lung adenocarcinoma cells in mice, suppressing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissues. Conclusion:Cholesterol may induce lung adenocarcinoma cells proliferation and metastasis by regulating the MYADM/Rac1/Akt/c-Myc/MCT1 axis.

OBJECTIVE To construct ensemble learning models for predicting high-use days of budesonide based on meteorological factors， thereby providing reference for hospital pharmacy management. METHODS Meteorological data for 2024 and outpatient budesonide usage data from the jurisdiction of Sanming Hospital of Integrated Traditional Chinese and Western Medicine were collected. High-use days were defined as the 75th percentile of outpatient budesonide usage， and a corresponding dataset was established. The prediction task was formulated as a classification problem， and three ensemble learning models were developed： Random Forest， Extreme Gradient Boosting （XGBoost）， and Histogram-based Gradient Boosting Classifier. Model performance was evaluated using accuracy， precision， recall， F1-score， and log-loss. Model interpretability was analyzed using Shapley Additive Explanations （SHAP）. RESULTS The Histogram-based Gradient Boosting Classifier achieved the best performance （accuracy＝0.75， F1-score＝0.48）， followed by XGBoost （accuracy＝0.74， F1-score＝0.43） and Random Forest （accuracy＝0.72， F1-score＝0.22）. SHAP results suggested that the prediction results of the last two models have the highest correction. CONCLUSIONS Ensemble learning models can effectively predict high-use days of budesonide， with the Histogram- based Gradient Boosting Classifier demonstrating the best predictive performance. Low temperature， high humidity， and low atmospheric pressure show significant positive impacts on the prediction of daily budesonide usage.

OBJECTIVE To explore the mechanism by which Gongfa Static Training regulates mitophagy through the PTEN-in-duced kinase 1(PINK1)/Parkin pathway in skeletal muscle insulin resistance in type 2 diabetes mellitus(T2DM).METHODS T2DM mouse model was established using a high-fat diet combined with streptozotocin(STZ)intraperitoneal injection.Mice were ran-domly divided into a model group,a metformin group,an aerobic exercise group,and a Gongfa Static Training group.The intervention effects of Gongfa Static Training were evaluated by measuring fasting blood glucose,Homeostatic Model Assessment of Insulin Resist-ance(HOMA-IR),glycated hemoglobin(HbA1c),lipid metabolism indicators,mitochondrial function in the gastrocnemius muscle,and the expression of PINK1 and Parkin-related genes and proteins.RESULTS Gongfa Static Training significantly reduced fasting blood glucose,HbA1c,and insulin resistance index in T2DM mice,improved lipid metabolism,and enhanced insulin sensitivity.It improved the structure and function of mitochondria in the gastrocnemius muscle by upregulating the mRNA and protein expression of PINK1 and Parkin.CONCLUSION Gongfa Static Training improves mitochondrial function and insulin resistance in the skeletal muscle of T2DM mice by regulating the PINK1/Parkin pathway.

Objective To establish and validate a human comfort evaluation method based on musculoskeletal activity in biomechanics.Methods Firstly,the limitations of current biomechanical-based comfort evaluation method were analyzed.Secondly,a new evaluation method based on musculoskeletal activity was proposed,which considered the influence of muscle and joint on comfort,and a comfort index was obtained.Finally,the firefighter's water belt rolling task was selected for verification.Results The comfort index derived from the improved musculoskeletal activity-based evaluation method was 0.74,which was lower than the comfort index of 0.82 obtained from the comfort based on muscle activity.The verification results aligned with the theoretical analysis.A questionnaire survey conducted on 43 firefighters showed that the subjective assessments gathered were consistent with the verification outcomes,further confirming the conclusion that the former method was more comprehensive and accurate.Conclusions Compared to the method that focuses exclusively on muscle activity,the comfort evaluation method that integrates both muscle and joint conditions not only more accurately reflects the actual state of the human body but also comprehensively identifies potential biomechanical risks,thereby demonstrating greater practical significance.